Vaccinations Flashcards
Briefly describe the disease caused by canine adenovirus type 1.
Contrast with the disease caused by CAV-2
- CAV-1 is the cause of infectious canine hepatitis
- CAV-2 causes respiratory disease in dogs and is genetically distinct from CAV-1
- Adenoviruses are resistant to environmental inactivation and can survive days in fomites
- Fomites are the likely source of natural infection
- The virus is widespread in the wild carnivore population
- The virus localises in the tonsils after natural infection - then regional lymph nodes, lymphatics and blood via the thoracic duct
- The virus spreads to the liver parenchymal cells, kidney and CNS (endothelial cells) are the main targets
- The virus is cytotoxic and can cause widespread necrosis with panlobular hepatic necrosis the major cause of death
- Chronic hepatic damage may occur with persistence of the virus particles in the hepatic parenchyma despite and adequate antibody response (chronic latent infection)
- Interstitial nephritis can occur due to tubular localisation of the virus
- Corneal oedema, anterior uveitis and potentially glaucoma can occur due to viral damage of the subcorenal endothelium
Describe and discuss the canine adenovirus - 1 and CAV-2 vaccination and protocol
- MLV CAV-2 strains are used in most vaccines
- CAV-1 vaccines caused post-vaccine concerns including potential localisation in the kidney and nephritis
- Inactivated vaccines were inferior and required adjuvants made them allergenic
- Parenteral CAV-2 vaccines generate a heterotypic antibody response that is cross-protective for CAV-1
- CAV-2 vaccine may produce mild respiratory signs if given intranasally or IV, though this is usually subclinical and mild
- Intranasal vaccination is protective for the respiratory disease
- Vaccination 3-4 weeks apart at 8-10 and 12-14 weeks provides long term immunity
- 3 yearly boosters are recommended
Discuss the eitiology and epidemiology of canine parvovirus enteritits
- CPV is a non-enveloped DNA containing virus
- Lack of envelope ensures they are extremely stable in the environment
- Belongs to the same subgroup as feline parvovirus
- Many mutations have occurred with the CPV-2a, 2b and 2c strains most prevalent today
- Maternal antibody can be protective
- Clinical disease is often most severe when there is concurrent infection with:
- Helminths
- Protozoa
- Enteric bacteria - clostridia, campylobacter, salmonella
- Highly contagious - mostly spread by contact with contaminated faeces
- Incubation period of 4-6 days with the newer strains
- Disease is most severe in neonates / rapidly growing dogs < 6 months of age
Describe the pathogenesis of canine enteric parvovirus infection
- Oronasal innoculation generally via exposure to contaminated faeces
- Virus replication begins in the oropharyngeal lymphoid tissue and spreads to the blood via the thoracic duct
- Eventual spread to the intestinal crypts via viraemia - this occurs 1-5 days after exposure
- The virus destroys the germinal epithelium of the intestinal crypts
- This leads to marked villi shortening due to impaired turnover
- Attacks the mitotically active precursors to the leukocytes and lymphoid cells
- Neutropenia and lymphopenia
- Secondary bacteraemia and endotoxemia can occur due to both above mechanisms
- Virus excretion from the intestine occurs within 3-4 days of exposure - often prior to the onset of clinical illness
- Development of local intestinal antibody is necessary to stop intestinal shedding of the virus
- Serum antibodies may be detected as early as 3-4 days post-infection
Describe the potential neurological signs with clinical canine parvovirus infection.
What are the most likely causes for the neurological signs?
- CPV may directly replicate in neurological tissues
- CPV DNA and mRNA have been identified in dogs without neurological signs
- CPV has been identified in a range of dogs with various neurological signs, though cause and effect is not always clear
- The changes such as cerebellar hypoplasia as seen in kittens are unlikely to be caused by CPV in dogs
- Most neurological signs are likely to be attributable to the systemic disease caused by CPV enteritis
- DIC / haemorrhage
- hypoglycemia - direct neurological damage
- endotoxemia / bacteremia
- Sepsis
- Acid-base / electrolyte disturbances
Descirbe the diagnostic tests available to assist in the diagnosis of canine parvovirus enteritis
- CPV is best diagnosed by organism detection tests
- Serological tests are less helpful as most dogs have been vaccinated
- ELISA
- Useful in-house at the onset of clinical disease
- Specific but poorly sensitive
- Virus is seldom detected past 10-12 days following natural infection
- Intermittent shedding can reduce the sensitivity of the assay
- Early antibody production may bind virus particles and result in false negative results
- Can detect the various strains and weak positives may be seen following vaccination
- Nucleic acid amplification - PCR
- Sensitive
- Real-time methods can give a quantitative estimate of viral DNA load
- Peak detection at ~10 days post infection and can persistently detect virus for up to 54 days (at low levels)
- Will detect vaccine virus in blood/faeces for up to 2 weeks
- Can be used to identify different strains in the field and to differentiate between field and vaccine strains
List (and briefly describe) the major therapeutic options for treatment of severe clinical canine parvovirus infection
Note the treatments that have been studied but not found to be of benefit
- IV fluids
- Balanced electolytes especially potassium and glucose
- Anti-microbials
- E.coli and C. Perfringens most common secondary infections
- Penicillin / aminoglycoside combination
- Third generation penicillin / cephalosporin
- Ampicillin, amoxicillin, cephtazidime, cephotaxime
- Quinolones - not in young growing dogs
- E.coli and C. Perfringens most common secondary infections
- Anti-emetics (some controversy)
- 5-HT3 receptor antagonists - ondansetron / dolasetron
- metoclopramide or prochlorperazine
- May not inhibit vomiting and may lead to hypotension
- Early feeding / enteral feeding
- When possible can reduce recovery time and minimise weight loss
- Feline interferon omega
- Survival benefit shown when started early
Not beneficial or limited evidence
- Hyperimmune plasma - may be beneficial
- Endotoxin anti-sera
- Oseltamivir (Tamiflu)
- G-CSF
Describe and discuss the canine parvovirus vaccination and recommended vaccination protocol
- Inactivated vaccines can produce only a short lived protective response from a single injection
- A second vaccine dise can improve the immune response which can last for ~15 months
- MLV attenuated vaccines provide superior immunity to inactivated virus vaccines
- Early immunity - as early as 3 days post vaccination
- Maternal antibody can interfere
- MLV particles can be shed in the faeces
- The MLV disease process parallels that of wild type infection
- A single vaccine produces long-lived immunity as shown by rechallenge data
- 3-7 years
- Vaccination is recommended at 6-8 weeks, then each 2-4 weeks until 16 weeks of age
- The variation depends on the relative risk of exposure and potential viral load
- Early finish vaccines (10 weeks) may not be protective 100% of the time due to persistence of maternal antibody
Describe and discuss the canine distemper virus vaccination and recommended vaccination protocol
- Maternal antibody is transferred in colostrum and has a half life of 8.4 days
- MDA are usually absent by 12-14 weeks
- Vaccines are given at 6-8 weeks and then each 3-4 weeks until 16 weeks of age
- Adequate immunity requires two doses of vaccine, despite the absence of maternal antibodies, 2-4 weeks apart
- Vaccination may provide protective antibodies for 3-7 years, however antibody titres alone are not predictive of immunity to clinical disease
- The most highly protective MLV are more likely to cause clinical illness, whereas they are also most likely to induce “sterilising immunity”
Describe and discuss the feline parvovirus vaccination and recommended vaccination protocol
- Maternal antibodies have a half life of ~9.5 days
- Successful vaccination requires a reduction in MDA which occurs from 6.8-18 weeks depending on the antibody titre in the queen and the transfer of colostrum
- Therefore in kittens from queens in endemic areas should have their final vaccination no earlier than 16 weeks of age
- Inactivated vaccines need a booster to provide adequate protection
- CMI has been demonstrated as early as 3-7 days post second vaccine
- Immunity can last for 7.5 years - long term
- MLV vaccine will produce a neutralising titre of 8-10 after a single vaccine - likely protective long term
- Booster is still recommended
- The vaccination program varies from client owned to shelter cats
- Shelter cats should be vaccinated earlier (from 4 weeks) and each 2-3 weeks thereafter while at risk of exposure until ~14-16 weeks.